The Effects of Mood and Stress on Cardiovascular Responses
Sadak, Christina Elisa
Smith, Barry D
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The "reactivity hypothesis" posits that elevations in cardiovascular reactivity may increase the risk of developing adverse cardiovascular events over time. Negative emotions and stress may exacerbate cardiovascular reactivity, as represented by increases in blood pressure and heart rate responses. However, prior studies have reported mixed results. Therefore the primary goal of the present study was to examine the effects of stimuli intended to elicit either sadness (negative mood induction) or mental stress (stressor tasks) on blood pressure and heart rate responses, in particular, when placed alongside each other in one experimental paradigm. One hundred and six participants were randomized to one of four conditions: Mood Induction (Sad or Neutral) Only or Mood Induction (Sad or Neutral) plus Stressor Tasks. Continuous measures of heart rate and blood pressure were collected, in addition to periodic self-report measurements of sadness and perceived stress. It was first hypothesized that participants in the Mood Induction plus Stressor Task conditions would exhibit greater blood pressure and heart rate responses than the participants in the Mood Induction Only conditions. It was also hypothesized that the elicitation of a negative emotion would not predict significant increases in blood pressure and heart rate. Third, it was hypothesized that the elicitation of a negative emotion would not affect the relationship between the stressor tasks and blood pressure and heart rate. Finally, it was hypothesized that males would exhibit greater blood pressure responses than female participants. Data were analyzed using reactivity scores in a series of statistical analyses. Results supported several of the hypotheses, confirming that certain stressor tasks significantly increase blood pressure and heart rate responses. Findings also provided evidence that a negative mood induction is associated with significant increases in blood pressure and heart rate responses, even though these responses may not be unique to this specific negative emotion. Implications for future work, including clinical applications, are discussed.